control of respiration 2/chemical control of respiration (R7) Flashcards
homeostasis
- stable internal environment
- essential for normal cell and body function
- body systems maintain homeostasis, which is essential for survival of cells that make up body systems which maintain homeostasis…
components of our bodies internal environment that must be maintained within narrow ranges
- concentration of water and electrolytes within and outside the cells
- pressures and volumes
- pH
- body temperature
- concentration of nutrients eg.glucose
- concentration of O2 and CO2
- concentration of waste products eg. urea
- > pH, and concentration of O2 and CO2 are examples of negative feedback systems
negative feedback systems
- primary type of homeostatic control system
- opposes initial change
examples of negative feedback system
- control of gases (O2 and CO2)
- control of pH (H+)
components of negative feedback system
- sensor (monitors magnitude of a controlled variable)
- control center (compares sensor’s input with a set point)
- effector/s (makes a response to produce a desired effect)
cycle/steps involved in negative feedback system
deviation in controlled variable -> detected by sensor -> which informs control center -> which sends instructions to effector (s) -> which brings about a compensatory response -> which results in restoration of controlled variable to normal -> this relieves the deviation in controlled variable and also leads to negative feedback to shut off the system responsible for the response
chemical control of respiration
- example of a negative feedback control system
- the controlled variables are the blood gas tensions, especially carbon dioxide
- chemoreceptors sense the values of the gas tensions
chemoreceptors
sense the values of the gas tensions
peripheral chemoreceptors
- situated in the carotid bodies and aortic bodies
- sense tension of oxygen, carbon dioxide and [H+] (H+ concentration) in the blood
central chemoreceptors
- situated near the surface of the medulla of the brainstem
- respond to the [H+] (H+ concentration) of the cerebrospinal fluid (CSF)
CSF
- cerebrospinal fluid
- separated from the blood by the blood-brain barrier
- relatively impermeable to H+ and bicarbonate
- CO2 diffuses readily
why is CSF less buffered than blood
- CSF contains less protein than blood therefore is less buffered than blood
- protein hemoglobin makes an excellent buffer, it can bind to small amounts of acid in the blood, helping to remove that acid before it changes the blood’s pH
- > protein binds to CO2 generated H+
- therefore because there is less Hb in CSF, then less excess H+ are binded and removed so the pH remains more acidic than returning to neutral
hypercapnia
increased arterial PCO2
hypercapnia (increased arterial PCO2) and ventilation
- the ventilation system is very responsive to PCO2 (due to the central chemoreceptors responding to levels of CO2 generated H+)
- as PCO2 increases, ventilation increases
controlled variables in chemical control of respiration (eg. of negative feedback system)
- decreased PO2
- increased arterial PCO2
- increased arterial [H+]
sensor in chemical control of respiration (eg. of negative feedback system)
chemoreceptors (peripheral and central)
control center in chemical control of respiration (eg. of negative feedback system)
respiratory centers
effector (s) in chemical control of respiration (eg. of negative feedback system)
respiratory muscles leading to changes in ventilation
hypoxic drive of ventilation
- the effect is all via the peripheral chemoreceptors (This response does not control ventilation rate at normal pO2, but below normal the activity of neurons innervating these receptors increases dramatically, so much so to override the signals from central chemoreceptors in the hypothalamus, increasing pO2 despite a falling pCO2)
- stimulated only when arterial PO2 falls to low levels (
hypoxia
decreased arterial PO2
hypoxia (decreased arterial PO2) and ventilation
-peripheral chemoreceptors are stimulated when PO2 falls to low levels (
what is hypoxia at high altitudes caused by
decreased partial pressure of inspired oxygen (PiO2)
PiO2
partial pressure of inspired O2
what is the acute response to hypoxia at high altitudes
- hyperventilation
- and increased cardiac output
what are the symptoms of acute mountain sickness (due to hypoxia at high altitudes)
- headache
- fatigue
- nausea
- tachycardia
- dizziness
- sleep disturbance
- exhaustion
- shortness of breath
- unconsciousness
PAO2 (alveolar gas equation)
- partial pressure of oxygen in the alveolar air
- PAO2= PiO2 - [PaCO2/0.8]
- PAO2= 150 - [40/0.8]
- PAO2=150-50 = 100mHg (13.3 kPa) at sea level
PiO2
=partial pressure of O2 in inspired air
- as the air in the respiratory tract is saturated with water, the water vapour pressure contributes about 47mmHg to the total pressure in the lungs
- therefore the pressure of inspired air = atmospheric pressure - water vapour pressure (760 - 47 = 713 mmHg at sea level)
- PiO2 would then = 713 x 0.21 = 150mmHg
PaCO2
partial pressure of CO2 in arterial blood
respiratory exchange ratio (RER)
=0.8
-ratio of CO2 produced/O2 consumed for someone eating a mixed diet
normal arterial PCO2
40mmHg
how would you use the alveolar gas equation to calculate the partial pressure of oxygen in alveolar air (PAO2) at the top of mount Everest for example
- you would have to be given the PiO2 (partial pressure of O2 in inspired air) and substitute it into the equation (PAO2= PiO2 - [PaCO2/0.8])
- PiO2 at the top of mount Everest = 43mmHg
PiO2 at sea level
150mmHg
chronic adaptations to high altitudes hypoxia
- increased RBC production (polycythaemia) which increases the O2 carrying capacity of blood
- increased 2,3 BPG produced within RBC which increases the ease at which O2 is offloaded into tissues
- increased number of capillaries which increases the ease at which blood diffuses
- increased number of mitochondria which means that O2 can be used more efficiently
- kidneys conserve acid which decreases the arterial pH causing an increased release of O2 (bohr effect)
H+ drive of respiration
- the effect is via the peripheral chemoreceptors
- H+ doesn’t readily cross the brain barrier (CO2 does)
- the peripheral chemoreceptors play a major role in adjusting for acidosis caused by the addition of non-carbonic H+ to the blood (eg.lactic acid during exercise; and diabetic ketoacidosis)
- their stimulation by H+ causes hyperventilation increases elimination of CO2 from the body (remember CO2 can generate H+ so its increase elimination helps reduce the load of H+ in the body)
- this is important in acid-base balance
acidosis
an excessively acid condition of the body fluids or tissues
neural and chemical factors that may increase ventilation during exercise
- reflexes originating from body movement
- adrenaline release
- impulses from the cerebral cortex
- increase in body temperature
- later: accumulation of CO2 and H+ generated by active muscles
effect of decreased PO2 in the arterial blood on the peripheral chemoreceptors
-stimulates only when the arterial PO2 has fallen to the point of being life threatening (
effect of decreased PO2 in the arterial blood on the central chemoreceptors
-directly depresses the central chemoreceptors and the respiratory center itself when
effect of increased PCO2 in the arterial blood and increased H+ in the brain ECF on the peripheral chemoreceptors
weakly stimulates
effect of increased PCO2 in the arterial blood and increased H+ in the brain ECF on the central chemoreceptors
- strongly stimulates, is the dominant control of respiration
- levels >70-80mmHg directly depress the respiratory center and the central chemoreceptors
effect of increased H+ in the arterial blood on the peripheral chemoreceptors
- stimulates
- important in acid-base balance
effect of increased H+ in the arterial blood on the central chemoreceptors
- does not affect
- cannot penetrate the blood-brain barrier
